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Goeders & Guerin (1994) point out that anxiety and stress may be involved in drug use and increased risk of dependency, as these are involved in the etiology of cocaine use. This is also supported by Carlson & Birkett (2021), describing a study where stressed rats became more sensitive to the effects of cocaine. Other evidence suggests that the earlier the stress, the greater the impact of long-lasting drug-taking behavior. Therefore, other factors contributing to stress, such as isolation, anxiety, and pain are evident factors. Furthermore, some elements of brain activity, such as a lower media prefrontal cortex function, are present in drug users.
Conflict experiments have been used since the mid-20th century to mimic human behavior in animals. Essentially for one component, a shock was delivered, while nothing was done for the other, creating a control group type of situation. This conflict paradigm is meant to create a stress-like response in animals that humans would face in order to devise a reliable methodology for screening for anxiolytic drug activity. Once the shocks were administered, it would create behavior change in the animals, and the drug was administered to determine if changes out occur (Goeders & Guerin, 1994).
Goeders and Guerin (1994) designed the experiment to test the effect of both predictable and unpredictable stress. The shock contingent first group of rats received a shock every time they pressed a lever for food, reinforced during the first part of the experiment. Meanwhile, the shock non-contingent rats in the second group would receive the shock as well upon the first group pressing the lever. However, unlike the first group, their shock was not related to food nor initiated by their actions, so it was essentially random. This created the so-called conflict paradigm and a high-stress situation. Since the rats were then given the option to self-administer cocaine at varying doses, the goal was to identify whether the contingency changed the behavior of rats in terms of substance abuse. Carlson & Birkett (2021) highlight that reinforcement plays a direct role in substance abuse, as both positive and negative reinforcement contributes to its development. The reinforcement of stimulus occurs immediately after a response, which is why many drug users prefer not necessarily more potent drugs but ones that work quickly. Negative reinforcement is a behavior that reduces an aversive stimulus will also be reinforced. Therefore, when the rats were randomly shocked, without the prior stimuli of food, they likely experienced some level of pain, and were offered cocaine. The cocaine masked the pain and stimulated pleasure centers, reducing the aversive stimulus and generating addiction.
The results of Goeders & Guerin (1994) determined that the rats in the non-contingent independent foot shock group self-administered the largest amount of cocaine. The acquired cocaine in low doses but high frequency before maxing out. The contingent group was second in self-administration, while the third control no shocks group was also the lowest in self-administration. Given the set-up of the experiment, it seems the no-shock group was meant to recreate a no-stress control environment, one where no stimulation was applied to the rats. The study premise was that some individuals could use cocaine recreationally, without addiction, while others see escalating patterns of use, whereas, like in the non-contingent group, the amount no longer mattered as long as a dose could be attained. Stress-induced environment and anxiety are variables that potentially influence the behavioral and neurobiological variables responsible for this control. Therefore, the potential outcome is whenever an individual is more susceptible to stress, the greater the possibility of addiction.
References
Carlson, N.R., & Birkett, M. (2021). Foundations of behavioral neuroscience (10th ed.). Pearson.
Goeders, N. E., & Guerin, G. F. (1994). Non-contingent electric footshock facilitates the acquisition of intravenous cocaine self-administration in rats. Psychopharmacology, 114(1), 6370. Web.
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